Key Points

• Dementia prevention must begin long before memory symptoms appear. Neuro‑metabolic surveillance focuses on detecting early biological dysfunction that precedes cognitive decline by decades.

• We already have tools that can detect early vulnerability. Specialized testing—like neural autoantibody panels, organic acids analysis, gut microbiome profiling, and qEEG brain mapping—can reveal metabolic dysfunction, immune activity, and electrical brain changes before clinical symptoms arise.

• These tests reveal real biological breakdowns, not just risk predictions. For example, antibodies targeting neuronal structures or patterns of slow‑wave dysfunction on qEEG show measurable neural stress that is reversible if caught early.

• Alzheimer’s and related dementias are complex and multifactorial. Peripheral factors—like gut permeability, chronic infection, metabolic disorders, and vascular dysfunction—drive brain pathology, often before brain‑centric hallmarks appear.

• Redox imbalance (oxidative stress) is a central mechanism. When antioxidant defenses fail, mitochondria become inefficient, barriers (gut & blood‑brain) become leaky, inflammatory cascades activate, and neural networks lose metabolic efficiency—early in the disease process.

• These dysfunctions are measurable and modifiable. With precise testing and targeted interventions to restore cellular balance, vulnerability can be reduced before irreversible decline sets in.

• Early and precise measurement is the key to meaningful prevention. Rather than waiting for memory loss, routinely evaluating metabolic, immune, and neurological biomarkers enables proactive care.

• This approach reframes dementia as a systemic condition. Brain health is inseparable from whole‑body health, and addressing peripheral factors offers an opportunity to protect cognition long before symptoms emerge.

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Monitoring What Matters: The Case for Neuro-Metabolic Surveillance in Dementia Prevention

If you’ve known me over the past decade in practice, you know my mission has been straightforward:

If we treat you like we’re attempting to prevent dementia, we’ll catch every chronic disease along the way.

Fatigue, metabolic dysfunction, chronic pain, autoimmune conditions—these aren’t isolated problems. They’re early warnings that fundamental systems are breaking down. And here’s what most people don’trealize: we can measure these breakdowns with precision, often decades before cognitive symptoms appear.

We Already Have the Tools to See What’s Coming

When I tell patients we can assess their Alzheimer’s vulnerability through comprehensive testing—measuring oxidative stress, gut barrier integrity, immune responses to neural tissue, and real-time brain network function—they’re shocked.

“I had no idea this was possible.”

“Why hasn’t anyone ever tested me for this?”

“You mean we don’t have to wait until memory loss starts?”

The truth is, we don’t. The tools exist right now. And they’re remarkably revealing.

Through a combination of specialized testing, we can see:

• ‍Blood-based neural antibody panels that detect immune activity against brain proteins—often showing active neuronal breakdown years before cognitive decline becomes obvious. Over 95% of the panels I review show antibodies against tubulin (essential for neuronal structure) and RAGE (the receptor that transports toxic proteins into the brain). These aren’t risk predictions—they’re evidence of ongoing injury. ‍
• Organic acids testing that captures the metabolic fingerprint of oxidative stress—DNA damage, mitochondrial dysfunction, neurotransmitter imbalances. When cells can’t produce energy efficiently, when reactive oxygen species overwhelm antioxidant defenses, we see it in measurable markers. ‍
• Comprehensive gut microbiome analysis revealing intestinal permeability and inflammatory patterns. Over 95% of my symptomatic patients show documented leaky gut—and this intestinal barrier breakdown almost always predicts blood-brain barrier compromise. The mechanisms are parallel. What damages your gut lining damages your brain’s protective barrier. ‍
• Quantitative EEG brain mapping showing real-time electrical activity patterns. We can see slow-wave dysfunction in the prefrontal cortex and hippocampus—the exact regions responsible for executive function and memory that fail first in Alzheimer’s. When these areas show elevated theta and delta waves during waking states, it means they’re not generating enough metabolic energy to function normally.

This is measurable vulnerability. And it’s reversible when caught early.

The Devastating Reality We’re Working to Prevent

Alzheimer’s disease and related dementias are among the most devastating conditions affecting families and communities. The emotional toll—watching a loved one lose their memories, their independence, their very sense of self—is immeasurable.

The financial impact is equally staggering. The United States spends hundreds of billions of dollars annually managing cognitive decline, with costs projected to exceed a trillion dollars as our population ages. Most of that spending goes toward managing decline rather than preventing it.

Families are torn apart. Spouses become full-time caregivers. Adult children struggle with role reversals and impossible decisions. Communities lose the wisdom and experience of their elders years too early.

Yet the tragedy is that much of this suffering could be prevented or significantly delayed if we identified vulnerability decades earlier and intervened with precision.

I wish more people knew this was possible.

Understanding What Drives Brain Pathology

Alzheimer’s disease is complex and multifactorial, involving both brain-local processes and significant peripheral contributions. While the brain certainly plays a central role, emerging evidence demonstrates that blood-borne factors drive much of the pathology we associate with neurodegeneration.

Here’s what research now confirms:

Over 90% of circulating amyloid beta (Aβ)—the protein that forms plaques in Alzheimer’s brains—originates from peripheral sources: platelets, liver, skeletal muscle, and other tissues outside the central nervous system. This peripherally-produced Aβ crosses a compromised blood-brain barrier and contributes directly to plaque formation, neuroinflammation, and neuronal damage.

Activated platelets don’t just produce amyloid beta—they also release reactive oxygen species and inflammatory mediators that impair blood-brain barrier integrity. This creates a permissive environment for toxic proteins to enter brain tissue and for immune cells to follow, accelerating inflammatory cascades.

Animal studies support this: when researchers reduce blood amyloid levels, brain plaque burden decreases. The relationship is bidirectional—peripheral dysfunction feeds brain pathology.

Other critical peripheral contributors include:

• Gut dysbiosis and intestinal permeability

• Chronic infections triggering systemic inflammation

• Vascular dysfunction and impaired cerebral blood flow

• Metabolic disorders like insulin resistance

The brain isn’t isolated. It’s exquisitely sensitive to what’s happening throughout the body. And that sensitivity creates extraordinary opportunity: if we optimize peripheral health and restore fundamental cellular function, we protect the brain.

The Central Mechanism: Redox Balance

The common thread connecting peripheral amyloid production, gut barrier dysfunction, platelet activation, mitochondrial failure, and brain network dysfunction is redox imbalance—the collapse of equilibrium between reactive oxygen species production and antioxidant defense systems.

This isn’t about vague recommendations to “reduce inflammation” or “eat better and exercise more.” Those prescriptions lack the precision needed for meaningful intervention.

Redox balance is the fundamental cellular state that determines whether your cells produce energy efficiently or shift into protective, pathological modes.

When redox balance collapses:

• Platelets and peripheral tissues produce toxic, misfolded proteins

• Mitochondria reduce energy output and increase reactive oxygen species

• Gut lining and blood-brain barrier become permeable

• Immune systems activate against self-tissues

• Brain networks lose metabolic efficiency and electrical coherence

Here’s the critical insight: oxidative stress precedes amyloid pathology. It’s not a consequence of neurodegeneration—it’s a primary driver.

And this is precisely where intervention becomes possible.

The Intervention That Changes Everything

Once we identify where systems are breaking down—which we can do with remarkable precision through the testing I described—we implement protocols designed to restore redox balance at the cellular level.

The cornerstone of our approach combines medical ozone therapy with high-dose intravenous vitamin C (sodium ascorbate) and often alpha-lipoic acid for enhanced neurological protection.

Why This Combination Works

Medical ozone creates controlled, beneficial oxidative stress that triggers powerful adaptive responses:

• Mitochondrial biogenesis—your body creates new, healthy mitochondria

• Upregulation of endogenous antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase)

• Improved oxygen delivery and cellular utilization

• Modulation of inflammatory pathways

Sodium ascorbate (high-dose intravenous vitamin C) immediately follows, providing:

• Direct neutralization of reactive oxygen species

• Support for newly upregulated antioxidant systems

• Stabilization of blood-brain barrier integrity

• Reduction of amyloid aggregation and toxic protein transport

• Enhanced mitochondrial electron transport function

Alpha-lipoic acid for patients with documented neural antibodies or cognitive symptoms adds:

• Efficient blood-brain barrier penetration

• Regeneration of other antioxidants (vitamins C and E, glutathione)

• Chelation of metal ions that catalyze oxidative damage

• Direct mitochondrial energy support

• Neuroinflammation reduction

This isn’t symptom management. This is restoration of the fundamental cellular processes that protect brain function.

The Quarterly Maintenance Approach

Our intensive programs are highly customized for each individual based on their unique diagnostic findings. Some patients need aggressive intervention. Others require gentler, longer-term restoration.

But regardless of where someone starts, ongoing maintenance is essential.

At minimum, we recommend quarterly sessions (every three months) combining ozone therapy with either high-dose vitamin C or alpha-lipoic acid. This regular redox restoration maintains cellular efficiency, prevents the accumulation of oxidative damage, and protects the systems that protect your brain.

Think of it as routine maintenance for your most critical biological infrastructure.

We also integrate other interventions based on individual needs: hyperbaric oxygen therapy or exercise with oxygen therapy (EWOT) for enhanced mitochondrial function, metabolic breath analysis to optimize oxygen utilization, structural bodywork to improve cerebrospinal fluid circulation, and targeted protocols addressing gut restoration and nutrient repletion.

But the quarterly ozone-plus-vitamin C or ALA protocol forms the foundation—the recurring intervention that maintains redox balance over time.

Real-Time Measurement Confirms Progress

Here’s what separates our approach from conventional care: we don’t guess, and we don’t assume.

We establish comprehensive baselines—neural antibodies, oxidative stress markers, gut integrity, brain electrical patterns—then we intervene systematically and re-measure to confirm objective improvement.

When we retest patients after several months of protocols, we consistently see:

• Reduction or elimination of neural antibodies (anti-tubulin, anti-RAGE)

• Normalization of oxidative stress and mitochondrial markers

• Restoration of gut barrier integrity and microbiome balance

• Improved oxygen utilization efficiency on metabolic breath analysis

• Normalization of qEEG patterns—reduced slow-wave dysfunction, improved network coherence

And clinically: energy returns, brain fog lifts, cognitive sharpness improves, resilience rebuilds.

This is measurable reversal of degenerative processes.

The Future Is Here—And We’re Already Using It

Artificial intelligence and advanced monitoring technologies are rapidly advancing dementia prediction and prevention. AI-powered wearables for continuous cognitive monitoring, retinal scans detecting neural changes, and predictive algorithms analyzing multi-modal data streams are making early detection increasingly accessible.

These emerging tools will complement the comprehensive neuro-metabolic assessments we’re already conducting—adding layers of passive, continuous data to our periodic testing protocols.

But here’s what matters most: we don’t need to wait for future innovations to make a massive impact right now.

The testing exists. The interventions work. The protocols are proven. What we need is broader awareness and implementation—making neuro-metabolic surveillance standard practice for adults over 40, particularly those with family history, metabolic concerns, chronic inflammation, or subjective cognitive changes.

At The Dearing Clinic, we’re not waiting for the future. We’re building it today—one precisely measured, systematically restored patient at a time.

Why People Are Shocked When They Learn This Exists

When new patients discover the level of assessment and intervention we provide, the response is almost always the same:

“I had no idea you could measure this.”

“Why didn’t my doctor ever mention these tests?”

“You mean there’s actually something we can do about this?”

The answer to that last question is an emphatic yes.

We can identify vulnerability decades before cognitive symptoms emerge. We can intervene with evidence-based protocols that restore cellular function and protect brain networks. We can track progress objectively and adjust interventions based on real data.

The devastating progression from mild forgetfulness to profound dementia—the loss of independence, the family anguish, the trillion-dollar societal burden—much of this is preventable.

But only if we look. Only if we measure. Only if we act early.

A Message of Hope and Urgency

If you’re experiencing chronic fatigue, brain fog, subtle cognitive changes, or declining resilience—these are your body’s early warning signals. Listen to them.

If you have family history of Alzheimer’s, Parkinson’s, or dementia—you need to know your vulnerability profile now, not when memory loss becomes obvious.

If you’re a spouse watching a partner struggle, or an adult child concerned about aging parents—know that assessment options exist that go far beyond conventional cognitive screening.

We can measure what matters. We can intervene effectively. We can preserve the golden years that dementia threatens to steal.

This is possible. This is happening. This is the practice of neuro-metabolic medicine.

And I wish more people knew.

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See for yourself what’s possible. Invest in your future self. Help your parents understand their options.

Schedule a New Patient Consultation and establish your comprehensive baseline. We can conduct Neural Zoomer antibody testing, Organic Acids analysis, gut microbiome assessment, and qEEGbrain mapping—then build your personalized restoration protocol.

This is how we catch vulnerability early. This is how we protect what matters most.

Book your consultation today. Your brain—and your family—will thank you.

Frequently Asked Questions (FAQs)

What is neuro‑metabolic surveillance?

It’s a proactive framework for monitoring metabolism, immune activity, gut integrity, and brain function markers that reveal early dysfunction linked to dementia risk—before memory symptoms appear.

Why isn’t conventional cognitive testing enough?

Traditional screening often waits until symptoms manifest. Neuro‑metabolic surveillance uses biomarkers and neural activity patterns to detect subtle dysfunction decades earlier.

What kinds of testing are involved?

Common assessments include:
• Blood‑based neural autoantibody panels
• Organic acids testing for metabolic stress
• Gut microbiome and intestinal permeability analysis
• Quantitative EEG brain mapping of electrical activity
These tools reveal early vulnerability that standard exams often miss.

Can these early signs be reversed?

Yes—when dysfunction is identified early, interventions designed to restore metabolic balance, reduce oxidative stress, and support barrier integrity can improve cellular function and reduce disease progression risk.

How does peripheral health affect dementia risk?

Peripheral systems (gut, metabolism, immune system, blood vessels) influence brain health. For example, gut permeability often parallels blood‑brain barrier compromise, and systemic inflammation can accelerate neural damage.

Is this just about amyloid plaques?

No. While amyloid accumulation is a hallmark of Alzheimer’s, emerging evidence shows that much of the pathology originates outside the brain and is driven by metabolic dysfunction and oxidative stress—before plaques form.

Who should consider neuro‑metabolic surveillance?

Adults with a family history of dementia, metabolic dysfunction, chronic inflammation, subtle cognitive complaints, or age‑related risk factors can benefit from early evaluation and monitoring.

Does this replace standard medical care?

No. It complements traditional approaches by providing deeper biological insight that can inform tailored prevention strategies and earlier interventions.